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Enoxacin extends lifespan of C. elegans by inhibiting miR-34-5p and promoting mitohormesis. | LitMetric

Enoxacin extends lifespan of C. elegans by inhibiting miR-34-5p and promoting mitohormesis.

Redox Biol

Department of Biophysics, Program in Molecular Biology, São Paulo School of Medicine, Federal University of São Paulo (UNIFESP), São Paulo, SP, Brazil; Laboratory of Aging Biology (LaBE), Department of Biochemistry and Tissue Biology, Program in Genetics and Molecular Biology, Institute of Biology, University of Campinas (UNICAMP), Campinas, SP, Brazil. Electronic address:

Published: September 2018

AI Article Synopsis

  • Alterations in miRNA processing relate to aging; the study used enoxacin to investigate its effects on aging in C. elegans, showing it can extend lifespan and enhance survival under stress.
  • The longevity effects of enoxacin depend on the transcription factor SKN-1/Nrf2 and are linked to the miRNA pathway, particularly the down-regulation of miR-34-5p, which plays a crucial role in this process.
  • Enoxacin's lifespan extension mechanism involves a prooxidant response and suggests potential new targets like double-stranded RNA-specific adenosine deaminases (ADARs) in the context of aging research.

Article Abstract

Alterations in microRNA (miRNA) processing have been previously linked to aging. Here we used the small molecule enoxacin to pharmacologically interfere with miRNA biogenesis and study how it affects aging in C. elegans. Enoxacin extended worm lifespan and promoted survival under normal and oxidative stress conditions. Enoxacin-induced longevity required the transcription factor SKN-1/Nrf2 and was blunted by the antioxidant N-acetyl-cysteine, suggesting a prooxidant-mediated mitohormetic response. The longevity effects of enoxacin were also dependent on the miRNA pathway, consistent with changes in miRNA expression elicited by the drug. Among these differentially expressed miRNAs, the widely conserved miR-34-5p was found to play an important role in enoxacin-mediated longevity. Enoxacin treatment down-regulated miR-34-5p and did not further extend lifespan of long-lived mir-34 mutants. Moreover, N-acetyl-cysteine abrogated mir-34(gk437)-induced longevity. Evidence also points to double-stranded RNA-specific adenosine deaminases (ADARs) as new targets of enoxacin since ADAR loss-of-function abrogates enoxacin-induced lifespan extension. Thus, enoxacin increases lifespan by reducing miR-34-5p levels, interfering with the redox balance and promoting healthspan.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6037660PMC
http://dx.doi.org/10.1016/j.redox.2018.06.006DOI Listing

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